Dong Ming, Yu Xinxin, Chen Wanfang, Guo Zhenzhen, Sui Linlin, Xu Yuefei, Shang Yuhong, Niu Weidong, Kong Ying
College of Basic Medical Sciences, Dalian Medical University, Dalian, China.
Department of Obstetrics and Gynecology of Renal Disease, the First Affiliated Hospital of Dalian Medical University, Dalian, China.
Cell Physiol Biochem. 2018;49(3):884-898. doi: 10.1159/000493219. Epub 2018 Sep 5.
BACKGROUND/AIMS: Periapical periodontitis is caused by bacterial infection and results in both one destruction and tooth loss. Osteopontin (OPN) is a secreted phosphorylated glycoprotein that participates in bone metabolism.
Thirty-three patients with chronic periapical periodontitis and 10 patients who had undergone the orthodontic removal of healthy tooth tissue (control) at the periodontal ligament were investigated, and an animal model of mouse periapical periodontitis was established for an in vivo analysis. The relationship between OPN and bone destruction during periapical periodontitis was analyzed. Osteoblasts and osteoclasts were cultured in vitro and treated with lipopolysaccharide. An inhibitor of NF-κB was used to pretreat the transfected cells.
OPN increased osteoclast proliferation and differentiation, but reduced osteoblasts proliferation and differentiation. OPN activated the NF-κB pathway during periapical periodontitis and accelerated the transfer and phosphorylation of P65 from the cytoplasm to the nucleus.
This study demonstrated that OPN played important roles in the progression of periapical periodontitis, and a dual role in bone metabolism during periapical periodontitis, linking osteoclasts and osteoblasts. The underlying mechanism may be related to the NF-κB pathway.
背景/目的:根尖周炎由细菌感染引起,会导致骨质破坏和牙齿脱落。骨桥蛋白(OPN)是一种分泌型磷酸化糖蛋白,参与骨代谢。
对33例慢性根尖周炎患者和10例在牙周膜处正畸拔除健康牙齿组织的患者(对照组)进行研究,并建立小鼠根尖周炎动物模型用于体内分析。分析根尖周炎期间OPN与骨破坏之间的关系。体外培养成骨细胞和破骨细胞,并用脂多糖处理。使用NF-κB抑制剂对转染细胞进行预处理。
OPN增加破骨细胞增殖和分化,但减少成骨细胞增殖和分化。OPN在根尖周炎期间激活NF-κB通路,并加速P65从细胞质向细胞核的转移和磷酸化。
本研究表明,OPN在根尖周炎进展中起重要作用,在根尖周炎期间的骨代谢中起双重作用,连接破骨细胞和成骨细胞。其潜在机制可能与NF-κB通路有关。